Ranzolin Aline, Bohn Jussara Marilú, Norman Gary L, Manenti Euler, Bodanese Luis Carlos, von Mühlen Carlos Alberto, Staub Henrique Luiz
Hospital São Lucas, PUCRS, Porto Alegre, RS, Brazil.
Arq Bras Cardiol. 2004 Aug;83(2):141-4; 137-40. doi: 10.1590/s0066-782x2004001400005. Epub 2004 Aug 17.
To determine whether high levels of antibodies against the phospholipid beta2-glycoprotein I (beta2-gpI) cofactor are associated with an increase in the risk of acute myocardial infarction.
The study comprised 82 patients with acute myocardial infarction and 82 controls, who were assessed in regard to age, sex, race, hypertension, smoking, previous heart disease, history of diabetes mellitus, and hypercholesterolemia. The following antibodies were detected using immunoassay: anticardiolipin and anti-beta2-gpI IgA, IgG, and IgM. Adjusted odds ratios (OR) for risk factors were obtained through logistic regression.
The mean ages of the cases and controls were, respectively, 57.7 and 51.1 years (P=0.003). Men (P=0.005) and the white race predominated in both groups (P=0.798). Of the risk factors, a history of diabetes (OR=5.3; 95% CI: 1.9 to 14.9; P=0.001) and previous heart disease (OR=4.7; 95% CI: 2.0 to 10.7; P<0.001) were the most consistent associations with myocardial infarction. The frequency of anticardiolipin IgG, IgM, and IgA antibodies did not differ between cases and controls (P=1.000). Anti-beta2-gpI IgA antibodies were more frequent in cases than in controls (P=0.054). The adjusted OR for anti-beta2-gpI IgA antibodies was 3.4 (95% CI: 1.3 to 9.1; P=0.015).
Anti-beta2-gpI IgA antibodies, but not anticardiolipin antibodies, seemed to behave as independent risk factors for myocardial infarction, which may represent a link between autoimmunity and atherosclerosis in patients with acute myocardial infarction.
